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Nerve Cell restoring,[object Object],Burcu ÖZAY 060090301,[object Object],Begüm ÜZEL 060090313,[object Object],Candan Ece DURMUŞ 060090327,[object Object]
Nerve cell : neuron,[object Object]
Nerve cell,[object Object],The basic unit of the nervous system is a highly specialized cell, also known as a neuron. It's main purpose is to transport messages from one part of the body to another in the form of nerve impulses. Because of their highly specialized function, neurons have certain special characteristics.,[object Object]
Nerve cell,[object Object]
Neural network,[object Object]
synapse,[object Object]
synapse,[object Object]
synapse,[object Object]
communicaton,[object Object]
Electric zap,[object Object]
Welcome site,[object Object]
Kopyası kopyas artofnervepart23
Diseasesduetonervecelldamageordeath,[object Object]
[object Object],Demyelination is theloss of themyelinsheath  (The myelin helps the nerve impulses travel smoothly and quickly from one nerve to the next.  ) insulatingnerve fibers or axons. ,[object Object],myelinated axon electron micrograph,[object Object]
NervecellDamageDemyelination- MultipleSclerosis (MS),[object Object],When demyelination occurs, the nerve impulses can no longer travel smoothly throughout the nervous system. The destruction of the myelin is shown by scars or lesions along the axons. It has been found that sometimes even the axons can become damaged or destroyed as well.,[object Object]
NervecellDamageDemyelination- MultipleSclerosis (MS),[object Object],Whatcausesdemyelination:Iftheoligodendrocytes (producetheMyelinsheath) aredamagedonlypartialremyelinationmayoccur. Little is knownaboutthemechanismsinvolved in thisprocess. Theimmunesystemmayplay a role in demyelinationassociatedwithsuchdiseases, includinginflammationcausingdemyelinationbyoverproduction of cytokinesaresecretedbytheglialcells) . Thereareglialcellscalledastrocytes. Theseareresponsibleforthescartissuewhichforms in place of themyelin. Thescarsorlesionsalongtheaxoncannotperformthewaythemyelindoes.,[object Object],cytokin,[object Object]
[object Object],Alzheimer’s results in disappearance of neurons within the memory centers of brain (generally the temporal and parietal lobes), thereby causing memory loss. This loss of neurons is coupled with increasing presence of beta-amyloid plaques and tangles within the Alzheimer’s patient’s brain.,[object Object]
Treatmants,[object Object],Inducing nerve cells to grow new connections with other cells, thus improving communication between remaining healthy cells. a protein called “WAVE-1″ regulates the growth of structures called spines that ultimately connect nerve cells. This technique is especially good for Alzheimer’s disease,[object Object]
Treatmants,[object Object],Prolactinhormone, which increases in the body during pregnancy, is directly responsible for the formation of new myelin in the brains and spinal cords of pregnant mice. Further, when non-pregnant mice with MS-like lesions were injected with prolactin, their myelin was also repaired. Thissolution is goodespeciallyfor MS disease.,[object Object],Prolactinsecretingcells,[object Object]
Treatmants,[object Object],Scientistsbelievethatdamage can be reversedbyreplacinglostcellswithnewonesderivedfromcellsthat can matureintonervecells, calledneuralstemcells. Researchers can thentransplantculturedstemcellsintothebrain of an animal model andallowthebrain'sownsignalstodifferentiatethestemcellsintoneuronsorglia. Alternatively, thestemcells can be inducedtodifferentiateintoneuronsandgliawhile in theculturedish, beforebeingtransplantedintothebrain.,[object Object]
OursolutIon,[object Object]
OursolutIon,[object Object],Our future application is about nogogene.This gene belongs to the family of reticulon-encoding genes. Reticulons are associated with the endoplasmic reticulum, and are involved in neuroendocrine secretion or in membrane trafficking in neuroendocrinecells.There are three isoforms: Nogo A, B and C. Nogo-A has two known inhibitory domains including amino-Nogo, at the N-terminus and Nogo-66, which makes up the molecules extracellular loop. Both amino-Nogo and Nogo-66 are involved in inhibitory responses, where amino-Nogo is a strong inhibitor of neurite outgrowth, and Nogo-66 is involved in growth cone destruction.No-go Decay,[object Object]
OursolutIon,[object Object],A major field of research in the "RNA field" is the quality control of mRNA production.Remember from the central dogma:DNA=>RNA=>ProteinWhen "genes are activated", what is really going on is that a DNA segment (i.e. the gene) is copied into RNA, that is then processed to form messenger RNA (mRNA) in the nucleus. But what happens if the mRNA is misprocessed? Or what happens if a gene acquires a mutation resulting in aberrant mRNAs?,[object Object],The eukaryotic cell has various mechanisms to deal with any bad mRNA.,[object Object]
OursolutIon,[object Object],As we see this nogogene.We should stop this gene.So our future application is about blocking this gene.We created a experiment, we are going to take out the damaged gene then we need to find out the trigger nogo for to put down.Whenever we get those genes we will put these to petri cub for to enhance them.After we restore these damaged cells we have to put them back as soon as possible for application. ,[object Object]
Some of pointsthatwehavemantioned in ourpresentation (Nervecellrestoring) withourhandmadenervecell model.,[object Object]
Structure of NerveCell,[object Object],cytokin,[object Object],NOGO gene,[object Object],axon,[object Object],nucleus,[object Object],myelinsheat,[object Object],demyelinatedarea,[object Object],dendrites,[object Object]
NerveCellDiseases-DemyelinationEffect of Cytokin,[object Object],Ourimmunitysystemtraetsthedemyelinatedarealike a scarfandoverproducescytokin . ,[object Object],Cytokinstickstothedemyelinatedarea but it doesn’twork in thewaymyelindoes. Itinterruptstheelectrycityflow.,[object Object]
OurSolutionBlocking NOGO gene,[object Object],Blocking  NOGO gene allowsthenervecelltogenerate. Soifwecouldblockthis gene therewill be no damagednervetissuesanymore.,[object Object]
Linksthatweused,[object Object],http://schools-wikipedia.org/wp/c/Chemical_synapse.htm,[object Object],http://www.bem.fi/book/02/02.htm,[object Object],http://en.wikipedia.org/wiki/Nerve_regeneration,[object Object],http://www.tutorvista.com/science/nerve-cell-structure-and-function,[object Object],http://en.labs.wikimedia.org/wiki/Human_Physiology/Print_Version,[object Object],http://pages.towson.edu/bdevan/Brain%20transplant%20follow-up%20articles/Langston%20et%20al,%201999%20-%20evidence%20of%20active%20cell%20degeneration%20in%20human%20MPTP%20exposure.pdf,[object Object],http://eyedocnews.com/003408-can-stem-cells-be-used-to-treat-optic-nerve-damage/,[object Object],http://www.sciencedaily.com/releases/2007/02/070221071152.htm,[object Object],http://esciencenews.com/dictionary/nerve.cell.damage,[object Object],http://answers.yahoo.com/question/index?qid=20090403173542AACbJgh,[object Object],http://en.wikipedia.org/wiki/Neuron,[object Object],http://www.alzinfo.org/08/alzheimers/reversing-nerve-cell-damage,[object Object],http://www.scholarpedia.org/article/Adult_neurogenesis,[object Object],http://www.ucalgary.ca/news/feb2007/ms-hormone/,[object Object],http://www.biotech-weblog.com/50226711/nerve_and_brain_cell_damage_reversal.php,[object Object]

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